In order to successfully infect a cell an influenza virus needs a small collection of proteins that are absolutely essential, and it looks like at least 90% of all individual influenza virions is lacking at least one of them, weird huh? Influenza mutates extraordinarily fast in order to outrun the immune systems of its host populations, generating new patterns that its hosts’ immune systems haven’t seen before by the time they are exposed again next flu season, and it seems like this must be just a natural consequence of how it does that. These results do call for a re-orientation in how we see influenza infection, in addition to potentially infection by many phages, as they show that not only must new hosts be infected by a population of distinct virions but indeed also each cell.
Influenza Virus with its parts, Source: http://micro.magnet.fsu.edu/cells/viruses/influenzavirus.html
CB Brooke, WL Ince, et al. Published 2013 in J. Virol. doi: 10.1128/JVI.02284-12
Segmentation of the influenza A virus (IAV) genome enables rapid gene reassortment at the cost of complicating the task of assembling the full viral genome. By simultaneously probing for the expression of multiple viral proteins in MDCK cells infected at low multiplicity with IAV, we observe that the majority of infected cells lack detectable expression of one or more essential viral proteins. Consistent with this observation, up to ninety percent of IAV-infected-cells fail to release infectious progeny, indicating that many IAV virions scored as non-infectious by traditional infectivity assays are capable of single-round infection. This fraction was not significantly affected by target or producer cell type but varied widely between different IAV strains. These data indicate that IAV exists primarily as a swarm of complementation-dependent semi-infectious virions, and thus traditional, propagation-dependent assays of infectivity may drastically misrepresent the true infectious potential of a virus population.